Inhibitory action of the alpha 1-adrenergic receptor on growth hormone secretion in the dog.

Intravenous administration of methoxamine ( METHOX , 5 mg, iv), a specific alpha 1-adrenergic agonist, reduced baseline GH levels of four unanesthetized beagle dogs 45 and 60 min post-injection and completely abolished the GH-releasing effect of the alpha 2-adrenergic agonist clonidine ( CLON , 4/ micrograms/kg, iv). Prazosin (PRA, 0.1 mg/kg, iv), an alpha 1-adrenergic antagonist, administered before METHOX re-instituted the GH-releasing effect of CLON . METHOX administered at the starting of an arginine infusion (ARG, 10% solution, 3.3 ml/min X 30 min) reduced consistently the GH releasing effect of the latter while, conversely, pretreatment with PRA, strikingly potentiated the GH-releasing effect of the amino acid (2 dogs). METHOX did not alter the GH-releasing effect of human pancreatic GH-releasing factor (hpGRF-40, 1/microgram/kg, iv), though it consistently delayed the occurrence of the GH secretory peak following hpGRF-40. These data indicate that alpha 1-adrenergic receptors located in the central nervous system, inhibit in the dog tonic and stimulated GH secretion.